Stress and  Hypertension: Symptoms and Treatment

 

“Stress, “Pressure”, “Tension”, and “Anxiety” are often synonymous. Therefore, it is not surprising that hypertension is viewed by many as also being indicative of a state of increased emotional tension, anxiety, or stress. If such a connection does exist, which comes first? Could they have a common cause? Almost 100 years ago, one of the earliest studies of hypertensive men emphasized that “one finds an unusual frequency of those, who as directors of big enterprises, had a great deal of responsibility, and who, after long periods of psychic overwork, became nervous”.1 A debate over whether a particular “hypertensive personality” exists has gone on ever since. Some believe that patients with hypertension are characterized by a generalized state of increased anxiety, while others claim that feelings of suppressed anger are more common. A tendency towards submissiveness and introversion has also been suggested, and increased denial and resistance to pain have been reported in those with a family history of high blood pressure. How can such varied views be reconciled?

The most likely explanation is that what we call “essential hypertension” is neither a discrete disorder nor a distinctive diagnosis. It simply reflects the observation that systolic and/or diastolic pressure measurements are consistently elevated when taken under basal conditions, and not due to some underlying disorder such as coarctation of the aorta, unilateral renal disease, pheochromocytoma, or primary aldosteronism. Thus, what we commonly refer to as hypertension, is really more of a description than a diagnosis. This is somewhat analogous to the popular diagnosis of fever during the last century, for which a variety of non-specific therapies were advocated. It’s now quite obvious that fevers can have varied origins, ranging from viral and bacterial infections, to cancer and connective tissue disorders. Each of these requires very different types of drugs. Cortisone might be beneficial for a patient with a temperature of 104° due to systemic lupus, but lethal if the cause were tuberculosis. Proper treatment depends upon finding the source of an elevated temperature, rather than simply attempting to lower it. Time honored approaches such as aspirin and fluids can often reduce fever, but may not always be desirable. Fever can represent a purposeful response in certain circumstances. Indeed, decades ago, artificially induced fever therapy was often used to treat various disorders, ranging from rheumatoid arthritis, and syphilis, to cancer. Similarly, an elevated blood pressure may represent a desirable homeostatic shift that should not be corrected in some patients, since the cure may be worse than the condition.

There are other similarities between how fever was viewed in the last century and our current conceptualization of hypertension, both with respect to diagnosis and treatment. The first advice generally given to patients is to avoid salt and adhere to a low sodium diet, but this is usually not effective, save for some with a family history or certain genetic traits. For others, calcium deficiency appears to be the culprit, and hypertension improves following calcium supplementation. These individuals might actually worsen on a low sodium regimen, since this would sharply restrict the intake of dairy products, which are the major sources of dietary calcium. Elevated blood pressures can similarly be lowered in some patients by potassium and/or magnesium supplementation. As indicated, arbitrary and vigorous treatment of hypertension can backfire, particularly when its significance and cause are unknown. Reducing the sodium load with diuretics may increase risk for sudden death due to ventricular fibrillation triggered by the resultant hypokalemia. Several studies have shown that a reduction of diastolic blood pressure below 85 mmHg increases the risk for myocardial infarction. In elderly patients particularly, increased adverse events may also accompany aggressive attempts to lower blood pressure to arbitrarily defined “normal” ranges.

That hypertension may have many causes requiring very different treatments, is attested to by the more than 80 different prescription preparations currently available. Unfortunately we do not have any algorithm that allows us to predict with certitude, which medication will be the most effective in any given patient. Many have disturbing side effects that can significantly vitiate vitality and quality of life. Consequently, current guidelines recommend that safe, non-drug approaches, should be considered first, consistent with the Hippocratic dictum primum non nocere . These might include weight reduction, specific dietary interventions as noted above, jogging, walking, and various exercise regimens. Meditation, yoga and other stress reduction strategies may also provide benefits, but are less often advocated or pursued. This seems somewhat surprising, in view of the popular presumption that stress can cause hypertension, and the widespread use of rest, relaxation, and sedatives such as bromides and phenobarbital, prior to the availability of specific antihypertensive drugs.

There is little doubt that both physical and mental stress can cause significant elevations of blood pressure. Transient measurements in excess off 400/250 mmHg have been recorded in elite weight lifters as they perform the supreme Valsalva maneuver. Ambulatory blood pressure monitoring studies on workers reveal that the highest pressures are often seen during telephone conversations, especially when this involves some controversy. Lynch and co-workers have convincingly shown in extensive studies, that a rise in blood pressure promptly occurs as soon as we start to speak. Baseline levels, rate and loudness of speech, subject matter, and the relative social status of the audience, can all influence the magnitude of this elevation.2 Although such rises may be dramatic and even alarming, they appear to be normal reactions with little prognostic significance. Blood pressure also rises when deaf mutes communicate in sign language, but not when they move their hands in an equally vigorous, but meaningless fashion. It is of interest that schizophrenics tend to be hypotensive, and blood pressure rises do not occur or are minimal when they talk, possibly because they really are not communicating. However, following successful drug treatment, they do respond normally.3 These observations suggest that the increase in blood pressure associated with speech and communication is due more to emotional, rather than physical stress.

Various forms of the cold pressor test have been utilized to evaluate patients since the early part of this century. It was originally proposed that exaggerated blood pressure increases resulting from this combination of physical and mental stress might be predictive for future hypertension, but this has not been substantiated. However, there is no proof that increased or decreased blood pressure responses to stress have any health consequences. Of the various causes or contributors to hypertension, stress can be shown to aggravate almost all. This includes salt sensitive hypertension (in both humans and animals), obesity, caffeine consumption, cigarette smoking, excessive alcoholic intake, and especially hypertension in blacks. However, can chronic stress alone cause permanent hypertension? Job stress, as defined by high demand but little control, has been clearly shown to be associated with increased rates of hypertension and coronary heart disease. But what is the mechanism? The transient elevation of blood pressure that regularly occurs in response to stress is most likely due to increased sympathetic-adrenal medullary activities. Along with this, there is a heightened state of anxiety and tension. But which comes first? Evidence for increased sympathetic tone can be demonstrated in most hypertensives, and if persistent, some authorities believe this could result in hypertension. However, in those with co-existent anxiety, it is not clear whether both stem from a common cause, whether anxiety causes increased sympathetic tone, or whether the reverse might be true.

There have been several attempts to unravel these interrelationships, the major stumbling block being the ability to accurately measure levels of anxiety over protracted periods of time. The most common and cost effective approaches utilize questionnaires to assess various aspects of anxiety. However, all of these are subject to the usual problems that plague self report instruments because of personal bias, and the need to validate test retest scores to satisfy concerns about reliability. It is also not certain whether state anxiety measurements, which reflect the individual’s status at that particular moment, are preferable to ratings of trait anxiety, with respect to demonstrating a causal relationship with sustained hypertension. It is obvious that increased anxiety would normally be present in individuals in whom a deadly diagnosis such as cancer or AIDS had been confirmed. How often this might apply to patients following the diagnosis of hypertension, is less certain. Indeed, as noted previously, hypertensive patients may have a tendency to exhibit an unusual degree of denial, or lack of concern about their condition.

Some reports do suggest that fixed hypertension occurs more frequently in individuals with antecedent high anxiety levels over a protracted period of time. In one large prospective study with almost twenty year follow up, about half the participants eventually developed hypertension. In a subgroup of over 300 men aged 45-59, high anxiety ratings based on the Framingham tension scale at the time of initial evaluation proved surprisingly predictive for future hypertension.4 In terms of prognostic power, anxiety levels were second only to baseline systolic blood pressure. This finding was independent of other risk factors for hypertension, such as obesity and alcohol intake. In contrast to previously reported findings5 anger measurement levels showed no such relationship, although this may have been related to the questionnaires that were utilized. In another prospective 3-year study of almost 500 women, 7 developed hypertension requiring permanent medication. Here again, baseline systolic pressure and anxiety level scores had the greatest prognostic significance.6 These and other studies support the contention that high levels of chronic anxiety may produce increased sympathetic tone of sufficient degree and duration to result in sustained hypertension in certain individuals. Other factors may also be involved. It might be productive to determine whether such relationships occur more often in hypertensives who can be classified in terms of renin profiles, degree of insulin resistance, or other objective criteria. This might help to further delineate specific subgroups of hypertension, and gain insight into possible stress related mechanisms that could contribute to its development, persistence, severity, and complications. Although the issue is far from settled, it does appear that “too much”, or “hyper” tension, may be an appropriate description of not only the physical, but also the emotional characteristics, consequences, and possibly cause of this disorder – at least for certain patients. For a more detailed discussion of renin profiling as an aid to determine the most appropriate treatment of hypertension in any given patient see Interview with Dr. John Laragh. Additional information on the role of stress in hypertension and a novel treatment of hypertension without medication, see Interview with Dr. James Lynch.

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